Potential Residential Exposure to TRIs Chemicals during Pregnancy
Potential Residential Exposure to TRIs Chemicals during Pregnancy
Background: Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood.
Objectives: We aimed to evaluate whether mothers of childhood brain cancer cases had greater potential residential exposure to Toxics Release Inventory (TRI) chemicals than control mothers during pregnancy.
Methods: We included 382 brain cancer cases diagnosed at < 10 years of age from 1993 through 1997 who were identified from four statewide cancer registries. One-to-one matched controls were selected by random-digit dialing. Computer-assisted telephone interviews were conducted. Using residential history of mothers during pregnancy, we measured proximity to TRI facilities and exposure index, including mass and chemicals released. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression to estimate brain cancer risk associated with TRI chemicals.
Results: Increased risk was observed for mothers living within 1 mi of a TRI facility (OR = 1.66 ; 95% CI, 1.11–2.48) and living within 1 mi of a facility releasing carcinogens (OR = 1.72 ; 95% CI, 1.05–2.82) for having children diagnosed with brain cancer before 5 years of age, compared to living > 1 mi from a facility. Taking into account the mass and toxicity of chemical releases, we found a nonsignificant increase in risk (OR = 1.25 ; 95% CI, 0.67–2.34) comparing those with the lowest versus highest exposure index.
Conclusions: Risk of childhood brain cancers may be associated with living near a TRI facility ; however, this is an exploratory study and further studies are needed.
There is significant concern about exposure of the fetus to environmental pollutants, food additives, and drugs, which may reach the fetus through the mother and affect the brain at critical stages of development. The developing central nervous system (CNS) is much more susceptible to chemical exposures than the adult CNS, and the brain is also the major target of toxicity for congenital effects. Some toxic agents impenetrable to the adult brain freely enter the developing brain because the blood-brain barrier of the fetus is not fully developed and is not completed until approximately 6 months after birth (Adinolfi 1985; Johanson 1980; Rodier 1994, 1995). Exposures to chemicals early in life are likely to have a greater impact on health outcomes such as cancer, neurodevelopmental impairment, and immune dysfunction (Thomas 1995).
Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood. The best established environmental risk factor for childhood brain cancer is radiation exposure (Harvey et al. 1985; Kuijten and Bunin 1993; MacMahon 1962; Mole 1974; Ron et al. 1988). Therapeutic cranial irradiation (X rays) has repeatedly been linked to childhood brain cancer, whereas diagnostic X rays with their usual low dose and short exposure periods were not enough to result in disease outcome (Kuijten and Bunin 1993).
Some studies investigated the risk for childhood cancer and birth defects among people living near hazardous waste sites and as a result of chemical exposures from the environment. Residential location has been a concern because toxic chemicals in landfill may disperse into the air or soil, eventually leading to human exposure (Elliot et al. 2001). In Clinton County, Pennsylvania, increased risk for cancer death was observed near the Drake Superfund site (Budnick et al. 1984). Other studies have attempted to find a link between childhood cancers and residential proximity to hazardous waste sites, with mixed results (Knox 2000; White and Aldrich 1999). In the Dover Township casecontrol study, a significantly increased odds ratio was observed for potential exposure to ambient air pollutants among female children with leukemia. However, no significant risks were found for brain cancer (New Jersey Department of Health and Senior Services and Agency for Toxic Substances and Disease Registry 2003).
One source of information on environmental contaminants is the Toxics Release Inventory (TRI), which is managed by the U.S. Environmental Protection Agency (U.S. EPA 2006). The TRI was established by a mandate of the Emergency Planning and Community Right-To-Know Act (EPCRA) of 1986. The TRI database contains an annual report of chemical releases to the environment and transfers of chemicals to off-site locations. The TRI captures the mass of specific compounds released into the environment (routinely or by accident) and those otherwise managed as waste. The mass of compounds released is considered to be relatively constant over the reporting period because what is released routinely and as waste usually exceeds what is accidentally released. As of 2002, > 650 toxic chemicals and chemical compounds are required to be reported.
The TRI database has been used in several studies. A link to slight increases in risk for certain birth defects associated with toxic releases (Marshall et al. 1997) has been suggested, but potential links to childhood cancers have not yet been investigated. The most common use of the TRI database has been to add up the total mass of TRI chemicals released to identify the most problematic polluters. However, this method emphasizes volume without regard to toxicity or environmental fate. Further, the total mass of chemicals released does not equal actual concentrations in the environment nor actual exposures to populations (Neumann 1998).
Previous studies used several different methods of categorizing exposure. Marshall et al. (1997) evaluated the risk of CNS and musculoskeletal birth defects from exposure to solvents, metals, and pesticides from hazardous contaminant sites including TRI sites in New York State. This casecontrol study rated the probability of exposure as "high," "medium," "low," or "unknown" for each contaminant group, using a standard, 1-mi radius template divided into 25 sectors. The templates were centered on the geographic coordinates of each contaminant site, overlaying with residential address at birth. This study found that residing within 1 mi of a TRI facility that released solvents had a significantly elevated risk for CNS defects with an odds ratio (OR) of 1.3.
Neumann et al. (1998) attempted to create a method for incorporating the toxicity factors so that the TRI data are more useful in estimating concentrations in the environment and potential effects from exposure. The chronic toxicity index was developed by the U.S. EPA's Region III Air Radiation and Toxics Division using the TRI databases and chronic oral toxicity factors and total mass for both carcinogens and noncarcinogens to estimate the relative hazards of TRI chemicals. The investigators used oral reference doses and cancer potency factors for the chronic toxicity index and ranked TRI chemicals on the basis of total mass versus total chronic toxicity index. The results varied greatly (Neumann et al. 1998). Even though the chronic toxicity index has its own limitations, it is likely to be a better indicator of potential risk than the use of mass alone.
The primary objective of this study was to investigate whether mothers of childhood brain cancer cases had greater potential residential exposure to TRI chemicals than control mothers during pregnancy. We assessed potential exposure by considering residential proximity to TRI facility during pregnancy, whether carcinogens were emitted, and a comparative ranking system for TRI chemical releases by combining toxicity information and total mass of release.
Abstract and Introduction
Abstract
Background: Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood.
Objectives: We aimed to evaluate whether mothers of childhood brain cancer cases had greater potential residential exposure to Toxics Release Inventory (TRI) chemicals than control mothers during pregnancy.
Methods: We included 382 brain cancer cases diagnosed at < 10 years of age from 1993 through 1997 who were identified from four statewide cancer registries. One-to-one matched controls were selected by random-digit dialing. Computer-assisted telephone interviews were conducted. Using residential history of mothers during pregnancy, we measured proximity to TRI facilities and exposure index, including mass and chemicals released. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression to estimate brain cancer risk associated with TRI chemicals.
Results: Increased risk was observed for mothers living within 1 mi of a TRI facility (OR = 1.66 ; 95% CI, 1.11–2.48) and living within 1 mi of a facility releasing carcinogens (OR = 1.72 ; 95% CI, 1.05–2.82) for having children diagnosed with brain cancer before 5 years of age, compared to living > 1 mi from a facility. Taking into account the mass and toxicity of chemical releases, we found a nonsignificant increase in risk (OR = 1.25 ; 95% CI, 0.67–2.34) comparing those with the lowest versus highest exposure index.
Conclusions: Risk of childhood brain cancers may be associated with living near a TRI facility ; however, this is an exploratory study and further studies are needed.
Introduction
There is significant concern about exposure of the fetus to environmental pollutants, food additives, and drugs, which may reach the fetus through the mother and affect the brain at critical stages of development. The developing central nervous system (CNS) is much more susceptible to chemical exposures than the adult CNS, and the brain is also the major target of toxicity for congenital effects. Some toxic agents impenetrable to the adult brain freely enter the developing brain because the blood-brain barrier of the fetus is not fully developed and is not completed until approximately 6 months after birth (Adinolfi 1985; Johanson 1980; Rodier 1994, 1995). Exposures to chemicals early in life are likely to have a greater impact on health outcomes such as cancer, neurodevelopmental impairment, and immune dysfunction (Thomas 1995).
Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood. The best established environmental risk factor for childhood brain cancer is radiation exposure (Harvey et al. 1985; Kuijten and Bunin 1993; MacMahon 1962; Mole 1974; Ron et al. 1988). Therapeutic cranial irradiation (X rays) has repeatedly been linked to childhood brain cancer, whereas diagnostic X rays with their usual low dose and short exposure periods were not enough to result in disease outcome (Kuijten and Bunin 1993).
Some studies investigated the risk for childhood cancer and birth defects among people living near hazardous waste sites and as a result of chemical exposures from the environment. Residential location has been a concern because toxic chemicals in landfill may disperse into the air or soil, eventually leading to human exposure (Elliot et al. 2001). In Clinton County, Pennsylvania, increased risk for cancer death was observed near the Drake Superfund site (Budnick et al. 1984). Other studies have attempted to find a link between childhood cancers and residential proximity to hazardous waste sites, with mixed results (Knox 2000; White and Aldrich 1999). In the Dover Township casecontrol study, a significantly increased odds ratio was observed for potential exposure to ambient air pollutants among female children with leukemia. However, no significant risks were found for brain cancer (New Jersey Department of Health and Senior Services and Agency for Toxic Substances and Disease Registry 2003).
One source of information on environmental contaminants is the Toxics Release Inventory (TRI), which is managed by the U.S. Environmental Protection Agency (U.S. EPA 2006). The TRI was established by a mandate of the Emergency Planning and Community Right-To-Know Act (EPCRA) of 1986. The TRI database contains an annual report of chemical releases to the environment and transfers of chemicals to off-site locations. The TRI captures the mass of specific compounds released into the environment (routinely or by accident) and those otherwise managed as waste. The mass of compounds released is considered to be relatively constant over the reporting period because what is released routinely and as waste usually exceeds what is accidentally released. As of 2002, > 650 toxic chemicals and chemical compounds are required to be reported.
The TRI database has been used in several studies. A link to slight increases in risk for certain birth defects associated with toxic releases (Marshall et al. 1997) has been suggested, but potential links to childhood cancers have not yet been investigated. The most common use of the TRI database has been to add up the total mass of TRI chemicals released to identify the most problematic polluters. However, this method emphasizes volume without regard to toxicity or environmental fate. Further, the total mass of chemicals released does not equal actual concentrations in the environment nor actual exposures to populations (Neumann 1998).
Previous studies used several different methods of categorizing exposure. Marshall et al. (1997) evaluated the risk of CNS and musculoskeletal birth defects from exposure to solvents, metals, and pesticides from hazardous contaminant sites including TRI sites in New York State. This casecontrol study rated the probability of exposure as "high," "medium," "low," or "unknown" for each contaminant group, using a standard, 1-mi radius template divided into 25 sectors. The templates were centered on the geographic coordinates of each contaminant site, overlaying with residential address at birth. This study found that residing within 1 mi of a TRI facility that released solvents had a significantly elevated risk for CNS defects with an odds ratio (OR) of 1.3.
Neumann et al. (1998) attempted to create a method for incorporating the toxicity factors so that the TRI data are more useful in estimating concentrations in the environment and potential effects from exposure. The chronic toxicity index was developed by the U.S. EPA's Region III Air Radiation and Toxics Division using the TRI databases and chronic oral toxicity factors and total mass for both carcinogens and noncarcinogens to estimate the relative hazards of TRI chemicals. The investigators used oral reference doses and cancer potency factors for the chronic toxicity index and ranked TRI chemicals on the basis of total mass versus total chronic toxicity index. The results varied greatly (Neumann et al. 1998). Even though the chronic toxicity index has its own limitations, it is likely to be a better indicator of potential risk than the use of mass alone.
The primary objective of this study was to investigate whether mothers of childhood brain cancer cases had greater potential residential exposure to TRI chemicals than control mothers during pregnancy. We assessed potential exposure by considering residential proximity to TRI facility during pregnancy, whether carcinogens were emitted, and a comparative ranking system for TRI chemical releases by combining toxicity information and total mass of release.
Source...